Abstract
Trop2 is a cell-surface glycoprotein associated with epithelial carcinomas. Although recent studies indicated that Trop2 is expressed in some stem-like cells, the molecular function of the protein remains largely unknown. In the present study, we observed that acute phase myocardial infarction (MI) induced an increase of c-kit+/Trop2+ cells and found that Trop2 enhanced cardiac c-kit+ cell survival and proliferation via its antiapoptotic activity, due to an elevated activity of ribosomal S6 kinases in the mitogen-activated protein kinase pathway. This study provides insight into better understanding the molecular function of Trop2, which could serve as a potential target for the treatment of MI.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antigens, Neoplasm / chemistry
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Antigens, Neoplasm / metabolism*
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Apoptosis* / drug effects
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Apoptosis* / genetics
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Base Sequence
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Cell Adhesion Molecules / chemistry
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Cell Adhesion Molecules / metabolism*
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Cell Proliferation
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Cytokines / pharmacology
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Disease Models, Animal
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Gene Expression
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Gene Expression Regulation
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Gene Silencing
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Heart / drug effects
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Inflammation Mediators / pharmacology
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Male
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Mice
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Mitogen-Activated Protein Kinases / metabolism
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Myocardial Infarction / genetics
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Myocardial Infarction / metabolism*
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Myocardium / metabolism
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Myocardium / pathology
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Proto-Oncogene Proteins c-kit / metabolism*
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RNA, Small Interfering / chemistry
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RNA, Small Interfering / genetics
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Signal Transduction
Substances
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Antigens, Neoplasm
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Cell Adhesion Molecules
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Cytokines
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Inflammation Mediators
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RNA, Small Interfering
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TROP2 protein, mouse
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Proto-Oncogene Proteins c-kit
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Mitogen-Activated Protein Kinases